Matches in SemOpenAlex for { <https://semopenalex.org/work/W2018431270> ?p ?o ?g. }
Showing items 1 to 56 of
56
with 100 items per page.
- W2018431270 abstract "You have accessJournal of UrologyBladder and Urethra: Anatomy, Physiology and Pharmacology1 Apr 2011213 NEUROGENIC BLADDER CAUSES MARKED BLADDER REMODELING AND ALTERED PAIN RESPONSE IN MICE WITH EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS Andrew Horowitz, Cengiz Altuntas, Ahmet Ozer, Kenan Izgi, Fuat Bicer, and Firouz Daneshgari Andrew HorowitzAndrew Horowitz Cleveland, OH More articles by this author , Cengiz AltuntasCengiz Altuntas Cleveland, OH More articles by this author , Ahmet OzerAhmet Ozer Cleveland, OH More articles by this author , Kenan IzgiKenan Izgi Cleveland, OH More articles by this author , Fuat BicerFuat Bicer Cleveland, OH More articles by this author , and Firouz DaneshgariFirouz Daneshgari Cleveland, OH More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2011.02.323AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Multiple sclerosis (MS) is an inflammatory disease of the central nervous system which causes neurogenic bladder (NGB). Experimental autoimmune encephalomyelitis (EAE) mice have been widely used in MS research as they demonstrate similar T cell mediated demyelination and neurodegeneration. We have previously reported the evidence of NGB in EAE mice. The aim of this study was to examine the stages of neurologic deficit in relation to bladder remodeling, and examine the EAE mice responses to visceral pain. METHODS Female SJL mice (n=118) were immunized with mycobacteria tuberculosis along with Freund's adjuvant (control), and then of this sample, 100 mice were injected with myelin protolipid protein (PLP 139–151) to induce EAE. On days 0, 3, and 7 all mice received intraperitoneal injection of purified Bordetella pertussis toxin. Daily weights, and neurologic clinical scores (CS) were assessed for signs of neurodegeneration and graded as 1–5. Then, the animals were divided into two groups. The first group (n=42) was euthanized at 70 days, bladders were harvested and weighed, and then prepared with routine hematoxylin-eosin and Masson's trichrome staining. Digital imaging analysis was used to quantify bladder cross-sectional areas, and smooth muscle, urothelium, and collagen (Image-Pro Plus). The second group (n=76) was assessed after short and long term (day 70) for signs of neurodegeneration (CS 1–5), along with visceral pain responses from perpendicular pressure with calibrated von Frey hair monofilaments to the hind paw and supra-pubic region. RESULTS Significant increases in selective bladder areas of control compared to EAE (CS4) for total wall, urothelium, smooth muscle, collagen, and inner lumen (2.31 vs. 3.50, P=0.014; 0.3078 vs. 0.62, P=0.001; 1.49 vs. 2.00, P=0.036; 0.50 vs. 0.87, P=0.021; 0.22 vs. 0.71, P=0.001, respectively) were seen. Also noted were statistically significant increases from the outer perimeter (P=0.004), and percent of urothelium and collagen (P=0.0008 and P=0.004, respectively). Along with CS increase , the threshold response (>50%) to pain stimuli dramatically increased and visceral pain response decreased with short term supra-pubic area of 2.83g vs. 3.84g; and hind paw 3.61g vs. >4.56g (control vs. CS3, respectively). CONCLUSIONS EAE causes neurologic deficit in mice and contributes to marked bladder remodeling and a dramatic decrease in visceral pain response, which proportionally worsens as the neurodegeneration progresses. The EAE mouse could be used as a robust tool for studies of NGB. © 2011 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 185Issue 4SApril 2011Page: e88 Peer Review Report Advertisement Copyright & Permissions© 2011 by American Urological Association Education and Research, Inc.MetricsAuthor Information Andrew Horowitz Cleveland, OH More articles by this author Cengiz Altuntas Cleveland, OH More articles by this author Ahmet Ozer Cleveland, OH More articles by this author Kenan Izgi Cleveland, OH More articles by this author Fuat Bicer Cleveland, OH More articles by this author Firouz Daneshgari Cleveland, OH More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ..." @default.
- W2018431270 created "2016-06-24" @default.
- W2018431270 creator A5014935281 @default.
- W2018431270 creator A5016272612 @default.
- W2018431270 creator A5026426427 @default.
- W2018431270 creator A5081190453 @default.
- W2018431270 creator A5089084328 @default.
- W2018431270 creator A5000571776 @default.
- W2018431270 date "2011-04-01" @default.
- W2018431270 modified "2023-09-25" @default.
- W2018431270 title "213 NEUROGENIC BLADDER CAUSES MARKED BLADDER REMODELING AND ALTERED PAIN RESPONSE IN MICE WITH EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS" @default.
- W2018431270 doi "https://doi.org/10.1016/j.juro.2011.02.323" @default.
- W2018431270 hasPublicationYear "2011" @default.
- W2018431270 type Work @default.
- W2018431270 sameAs 2018431270 @default.
- W2018431270 citedByCount "0" @default.
- W2018431270 crossrefType "journal-article" @default.
- W2018431270 hasAuthorship W2018431270A5000571776 @default.
- W2018431270 hasAuthorship W2018431270A5014935281 @default.
- W2018431270 hasAuthorship W2018431270A5016272612 @default.
- W2018431270 hasAuthorship W2018431270A5026426427 @default.
- W2018431270 hasAuthorship W2018431270A5081190453 @default.
- W2018431270 hasAuthorship W2018431270A5089084328 @default.
- W2018431270 hasConcept C126322002 @default.
- W2018431270 hasConcept C142724271 @default.
- W2018431270 hasConcept C203014093 @default.
- W2018431270 hasConcept C2778486448 @default.
- W2018431270 hasConcept C2780640218 @default.
- W2018431270 hasConcept C529278444 @default.
- W2018431270 hasConcept C71924100 @default.
- W2018431270 hasConceptScore W2018431270C126322002 @default.
- W2018431270 hasConceptScore W2018431270C142724271 @default.
- W2018431270 hasConceptScore W2018431270C203014093 @default.
- W2018431270 hasConceptScore W2018431270C2778486448 @default.
- W2018431270 hasConceptScore W2018431270C2780640218 @default.
- W2018431270 hasConceptScore W2018431270C529278444 @default.
- W2018431270 hasConceptScore W2018431270C71924100 @default.
- W2018431270 hasIssue "4S" @default.
- W2018431270 hasLocation W20184312701 @default.
- W2018431270 hasOpenAccess W2018431270 @default.
- W2018431270 hasPrimaryLocation W20184312701 @default.
- W2018431270 hasRelatedWork W1763258797 @default.
- W2018431270 hasRelatedWork W1789772972 @default.
- W2018431270 hasRelatedWork W2065498976 @default.
- W2018431270 hasRelatedWork W2073510230 @default.
- W2018431270 hasRelatedWork W2079346212 @default.
- W2018431270 hasRelatedWork W2317531374 @default.
- W2018431270 hasRelatedWork W2506050086 @default.
- W2018431270 hasRelatedWork W4224868007 @default.
- W2018431270 hasRelatedWork W4319433888 @default.
- W2018431270 hasRelatedWork W97721380 @default.
- W2018431270 hasVolume "185" @default.
- W2018431270 isParatext "false" @default.
- W2018431270 isRetracted "false" @default.
- W2018431270 magId "2018431270" @default.
- W2018431270 workType "article" @default.